Pu-erh Tea Extract Attenuates Nicotine-Induced Foam Cell Formation in Primary Cultured Monocytes: An in Vitro Mechanistic Study

Tu, Shih Hsin; Chen, Ming‐Yao; Chen, Li Ching; Mao, Yi; Ho, Chi Hou; Lee, Wen Jui; Lin, Yen‐Kuang; Pan, Min‐Hsiung; Lo, Chih Yu; Chen, Chi Long; Yen, Yun; Whang‐Peng, Jacqueline; Ho, Chi Tang; Wu, Chih Hsiung; Ho, Yuan Soon

doi:10.1021/acs.jafc.6b00624

Cited by 9 publications

(9 citation statements)

References 38 publications

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“…Many kinds of natural compounds have been tested for their ability to inhibit a9-nAChR expression, and we found that inhibition of the signals induced by this receptor significantly diminished the effects of smoking [34–37]. Our previous study demonstrated that the estrogen-induced estrogen receptor is also promoted in nicotine-induced a9-nAChR activation [29].…”

Section: Discussionmentioning

confidence: 99%

Protein phosphatase Mg2+/Mn2+ dependent 1F promotes smoking-induced breast cancer by inactivating phosphorylated-p53-induced signals

Lin

Huang

et al. 2016

Oncotarget

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We previously demonstrated that the activation of α9-nicotinic acetylcholine receptor (α9-nAchR) signaling by smoking promotes breast cancer formation. To investigate the downstream signaling molecules involved in α9-nAChR-induced breast tumorigenesis, we used real-time polymerase chain reactions and Western blotting to assess expression of protein phosphatase Mg2+/Mn2+ dependent 1F (PPM1F), a Ser/Thr protein phosphatase, in human breast cancer samples (n=167). Additionally, stable PPM1F-knockdown and -overexpressing cell lines were established to evaluate the function of PPM1F. The phosphatase activity of PPM1F in nicotine-treated cells was assessed through Western blotting, confocal microscopy, and fluorescence resonance energy transfer. Higher levels of PPM1F were detected in the breast cancer tissues of heavy smokers (n=7, 12.8-fold) greater than of non-smokers (n= 28, 6.3-fold) (**p=0.01). In vitro, nicotine induced PPM1F expression, whereas α9-nAChR knockdown reduced the protein expression of PPM1F. A series of biochemical experiments using nicotine-treated cells suggested that the dephosphorylation of p53 (Ser-20) and BAX (Ser-184) by PPM1F is a critical posttranslational modification, as observed in breast cancer patients who were heavy smokers. These observations indicate that PPM1F may be a mediator downstream of α9-nAChR that activates smoking-induced carcinogenic signals. Thus, PPM1F expression could be used for prognostic diagnosis or inhibited for cancer prevention and therapy.

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Section: Discussionmentioning

confidence: 99%

Protein phosphatase Mg2+/Mn2+ dependent 1F promotes smoking-induced breast cancer by inactivating phosphorylated-p53-induced signals

Lin

Huang

et al. 2016

Oncotarget

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“…The key production process of pu-erh tea is secondary fermentation, in which microorganisms play a very important role in producing the taste, color, fragrance, and functional components 2 . Pu-erh tea is not only a popular tea, but also a traditional Chinese medicine, which has many biological and biochemical effects, such as antiobesity 3 , antiviral 4 , antioxidative 5 , hepatoprotective 6 , hypoglycemic 7 and hypolipidemic 8 . In our research, we found that the water extract of pu-erh tea showed potential in vitro hypoglycemic and hypolipidemic effects.…”

Section: Introductionmentioning

confidence: 58%

Flavanols from the Camellia sinensis var. assamica and their hypoglycemic and hypolipidemic activities

Wang

Liu

Zhu

et al. 2017

Acta Pharmaceutica Sinica B

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α-Glucosidase and lipase inhibitors play important roles in the treatment of hyperglycaemia and dyslipidemia. To identify novel naturally occurring inhibitors, a bioactivity-guided phytochemical research was performed on the pu-erh tea. One new flavanol, named (–)-epicatechin-3-O-(Z)-coumarate (1), and 16 known analogs (2—17) were isolated from the aqueous extract of the pu-erh tea. Their structures were determined by spectroscopic and chemical methods. Furthermore, the water extract of pu-erh tea and its fractions exhibited inhibitory activities against α-glucosidases and lipases in vitro; compound 15 showed moderate inhibitory effect against sucrase with an IC50 value of 32.5 μmol/L and significant inhibitory effect against maltase with an IC50 value of 1.3 μmol/L. Compounds 8, 10, 11 and 15 displayed moderate activity against a lipase with IC50 values of 16.0, 13.6, 19.8, and 13.3 μmol/L, respectively.

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“…Previous studies have demonstrated that Nic can be detected in the urine and plasma of the SHS, with less than 2 ng/ml for cotinine in urine and around 3 ng/ml in plasma . Moreover, direct exposure to NNK via cigarette smoking leads to detect NNK metabolite in plasma of smokers, range from Pico molar to Nano molar .…”

Section: Discussionmentioning

confidence: 99%

Long‐term exposure to extremely low‐dose of nicotine and 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK) induce non‐malignant breast epithelial cell transformation through activation of the a9‐nicotinic acetylcholine receptor‐mediated signaling pathway

Fararjeh

Chen

et al. 2018

Environmental Toxicology

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Breast cancer (BC) is the most common cancer affecting women worldwide and has been associated with active tobacco smoking. Low levels of nicotine (Nic) and 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK), have been detected in cases of second‐hand smoke (SHS). However, the correlation between SHS and BC risk remains controversial. In this study, we investigated whether the physiological SHS achievable dose of Nic and tobacco specific nitrosamine, NNK act together to induce breast carcinogenesis using an in vitro breast cell carcinogenesis model. Immortalized non‐tumorigenic breast epithelial cell line, HBL‐100 used for a time‐course assay, was exposed to very low levels of either Nic or NNK, or both. The time‐course assay consisted of 23 cycles of nitrosamines treatment. In each cycle, HBL‐100 cells were exposed to 1pM of Nic and/or 100 femtM of NNK for 48 hours. Cells were passaged every 3 days and harvested after 10, 15, and 23 cycles. Our results demonstrated that the tumorigenicity of HBL‐100, defined by soft agar colony forming, proliferation, migration and invasion abilities, was enhanced by co‐exposure to physiologically SHS achievable doses of Nic and NNK. In addition, α9‐nAChR signaling activation, which plays an important role in cellular proliferation and cell survival, was also observed. Importantly, an increase in stemness properties including the prevalence of CD44+/CD24− cells, increase Nanog expression and mammosphere‐forming ability were also observed. Our results indicate that chronic and long term exposure to environmental tobacco smoke, may induce breast cell carcinogenesis even at extremely low doses.

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Pu-erh Tea Extract Attenuates Nicotine-Induced Foam Cell Formation in Primary Cultured Monocytes: An in Vitro Mechanistic Study

Cited by 9 publications

References 38 publications

Protein phosphatase Mg2+/Mn2+ dependent 1F promotes smoking-induced breast cancer by inactivating phosphorylated-p53-induced signals

Protein phosphatase Mg2+/Mn2+ dependent 1F promotes smoking-induced breast cancer by inactivating phosphorylated-p53-induced signals

Flavanols from the Camellia sinensis var. assamica and their hypoglycemic and hypolipidemic activities

Long‐term exposure to extremely low‐dose of nicotine and 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK) induce non‐malignant breast epithelial cell transformation through activation of the a9‐nicotinic acetylcholine receptor‐mediated signaling pathway

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